Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0265264 (
HOS
)
1,119
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Osteosarcoma is a malignant tumor in children and adolescents. Previous studies showed that
ATG4A
is an autophagy-related gene involved in cancers. In this study, we aimed to identify the biological role of
ATG4A
in osteosarcoma. The expression levels of
ATG4A
were analyzed in osteosarcoma tissues by using reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and western blotting.
ATG4A
was knocked-down or overexpressed in SAOS2 and
HOS
cell lines by transfection. Cell counting kit-8 (CCK-8) and clone formation assay were used to assess the effects of
ATG4A
on cell proliferation. Wound healing and Transwell assays were performed to evaluate the effects of
ATG4A
on cell migration and invasion, respectively. Epithelial-mesenchymal transition (EMT) markers and Notch signaling pathway targeting molecules were examined by western blotting. The results indicated that
ATG4A
was up-regulated in osteosarcoma tissues. In SAOS2 cells, knockdown of
ATG4A
inhibited the proliferation, migration and invasion, up-regulated the expression of E-cadherin and down-regulated the expression of vimentin, Notch1 and Hes1. In
HOS
cells, overexpression of
ATG4A
promoted the proliferation, migration and invasion, up-regulated the expression of vimentin, Notch1 and Hes1 and down-regulated the expression of E-cadherin. In conclusion, these findings demonstrate that
ATG4A
is up-regulated in osteosarcoma tissues. In osteosarcoma cells,
ATG4A
promotes the EMT process partly by the Notch signaling pathway. These results suggest that
ATG4A
might represent a potential therapeutic target for patients with osteosarcoma.
...
PMID:Upregulation of ATG4A promotes osteosarcoma cell epithelial-to-mesenchymal transition through the Notch signaling pathway. 3196 49